Proteomic analysis reveals the protective effects of emodin on severe acute pancreatitis induced lung injury by inhibiting neutrophil proteases activity.

Abstract Acute lung injury (ALI) is the most common remote organ complication induced by severe acute pancreatitis (SAP). Almost 60–70% SAP-induced deaths are caused by ALI. Efficient clinical therapy strategy for SAP-induced ALI is still lacking. In this study, we demonstrate that Emodin (EMO) can significantly alleviate SAP-induced ALI. We investigate the therapeutic mechanisms of EMO by proteomic analysis, which indicates that EMO protects lung tissue against SAP-ALI by negative regulation of endopeptidase activity and inhibition of collagen-containing extracellular matrix degradation. Protein-protein interaction analyses showed LAMC2, Serpina1 and Serpinb1 to play important roles in the above pathways. This study elucidates the possible mechanism and suggests the candidacy of EMO in the clinical treatment of SAP-ALI. Significance ALI is a major leading cause of death in SAP. DEX is the standard of care drug for treatment of SAP-ALI, but often associated with inevitable side effects. In the present study, EMO was demonstrated to greatly alleviate the lung injury induced by SAP. Through proteomic analysis, the recovered protein profiles in response to EMO treatment in SAP-ALI rat models was obtained, among which LAMC2, Serpina1 and Serpinb1 were discovered as crucial regulatory proteins in SAP-ALI disease. Our study provides the underlying mechanisms and novel targets of EMO protective effect against SAP-ALI.